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1
Boers, G. H. J. Homocysttinuria: A risk factor of premature vascular disease. Dortrecht: Foris Publications, 1986.
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2
McKinley, Michelle. B-Vitamin status and plasma homocysteine: A risk factor for vascular disease. [S.l: The Author], 1999.
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3
Tousoulis, Dimitris. Risk factors and vascular endothelium. Hauppauge, N.Y: Nova Science Publishers, 2011.
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4
Jacobsen, Sarah R. Vascular dementia: Risk factors, diagnosis, and treatment. Hauppauge, N.Y: Nova Science, 2011.
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5
Román, Gustavo C. Managing vascular dementia: Concepts, issues, and management. London: Science Press, 2003.
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6
Andris, Kazmers, ed. Cardiac risk assessment before vascular surgery. Armonk, NY: Futura Pub. Co., 1994.
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7
M, Drance Stephen, ed. Vascular risk factors and neuroprotection in glaucoma: Update 1996. Amsterdam: Kugler Publications, 1997.
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8
Boers, G. H. J. Homocystinuria: A Risk Factor of Premature Vascular Disease. de Gruyter GmbH, Walter, 1986.
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9
Stewart, Robert. Vascular and mixed dementias. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0034.
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Vascular disease is the most important environmental risk factor for dementia but this research area has been hampered by inadequate outcome definitions – in particular, a diagnostic system that attempts to separate overlapping and probably interacting pathologies. There is now substantial evidence that the well-recognised risk factors for cardiovascular disease and stroke are also risk factors for dementia, including Alzheimer’s disease. However, these risk factors frequently act over several decades, meaning that the chances of definitive randomised controlled trial evidence for risk-modifying interventions are slim. This should not obscure the wide opportunity for delaying or preventing dementia through risk factor control and uncontroversial healthy lifestyles. Care should also be taken that comorbid cerebrovascular disease is not considered as excluding a diagnosis of Alzheimer’s disease, particularly now that this determines treatment eligibility.
10
Fromm, Annette. Vascular aetiology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.003.0004.
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Vascular aetiology of young ischaemic stroke covers a broad spectrum of causes. It includes the risk factor-mediated causes considered more common among the elderly on one hand, and a large number of rather rare disorders and conditions typical for younger ages on the other hand. This chapter is focused on atherosclerotic aetiology and comorbidity, small vessel disease and arterial dissection, which account for a majority of young ischaemic strokes worldwide, are treatable, and need to be considered as overall or contributing causes early during investigation. Specific and rare causes of young ischaemic stroke will be presented elsewhere.
11
Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Renal vascular disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0171.
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Renal vascular disease typically occurs with progressive narrowing of the main renal artery or smaller arterial vessels. Often, both patterns of disease coexist and result in ‘ischaemic nephropathy’ with damage to renal tissue. Much less commonly, inflammatory vasculitis can affect small or medium vessels. Ninety per cent of renal vascular disease is caused by atherosclerosis. Patients with renal vascular disease have an increased risk of cardiovascular death from associated cerebrovascular and coronary heart disease. Less than 10% of renal vascular disease is caused by fibromuscular dysplasia. The cause is unknown, but smoking is a risk factor. The disease is often bilateral and multifocal. It tends to affect the mid-portion of the renal artery, while atherosclerosis tends to occur at points of stress, especially at the junction of renal arteries with the aorta. This chapter reviews the diagnosis and management of renal vascular disease.
12
Guzik, Tomasz J., and Rhian M. Touyz. Vascular pathophysiology of hypertension. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0019.
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Hypertension is a multifactorial disease, in which vascular dysfunction plays a prominent role. It occurs in over 30% of adults worldwide and an additional 30% are at high risk of developing the disease. Vascular pathology is both a cause of the disease and a key manifestation of hypertension-associated target-organ damage. It leads to clinical symptoms and is a key risk factor for cardiovascular disease. All layers of the vascular wall and the endothelium are involved in the pathogenesis of hypertension. Pathogenetic mechanisms, whereby vascular damage contributes to hypertension, are linked to increased peripheral vascular resistance. At the vascular level, processes leading to change sin peripheral resistance include hyper-contractility of vascular smooth muscle cells, endothelial dysfunction, and structural remodelling, due to aberrant vascular signalling, oxidative and inflammatory responses. Increased vascular stiffness due to vascular remodelling, adventitial fibrosis, and inflammation are key processes involved in sustained and established hypertension. These mechanisms are linked to vascular smooth muscle and fibroblast proliferation, migration, extracellular matrix remodelling, calcification, and inflammation. Apart from the key role in the pathogenesis of hypertension, hypertensive vasculopathy also predisposes to atherosclerosis, another risk factor for cardiovascular disease. This is linked to increased transmural pressure, blood flow, and shear stress alterations in hypertension, as well as endothelial dysfunction and vascular stiffness. Therefore, understanding the mechanisms and identifying potential novel treatments targeting hypertensive vasculopathy are of primary importance in vascular medicine.
13
Landmesser, Ulf, and Wolfgang Koenig. From risk factors to plaque development and plaque destabilization. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0003.
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This chapter begins with a discussion of recent vascular research that has unveiled the complex interaction between exposure to risk factors and pathological changes at the vessel wall. Risk factors such as smoking or hyperlipidaemia first cause a pre-morbid phenotype with reversible dysfunction of flow-mediated vasodilation, known as endothelial dysfunction (ED). If exposure to risk factor(s) does not cease, ED develops into the first morphological vascular changes that finally lead to atherosclerosis. Cholesterol crystals have been shown to lead to pro-inflammatory activation of macrophages. Progression from stable coronary plaques to the plaque rupture that underlies the acute coronary syndrome is discussed in detail. The chapter provides a basic up-to-date concept of the development and progression of atherosclerosis and highlights the stages where preventive measures may still be effective.
14
Moulton, Calum D., and Clive Ballard. The association between depression and cognitive impairment in type 2 diabetes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198789284.003.0009.
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Type 2 diabetes (T2D) is an established risk factor for vascular dementia and Alzheimer’s disease, yet, the reasons are incompletely understood. To date, intervention studies targeting isolated risk factors, such as hypertension or hyperglycaemia, have proved unsuccessful. Several well-designed cohort studies have suggested that depression predicts cognitive decline in patients with T2D. However, these studies, all of later-life depression, have not fully excluded the potential for clinical overlap between depression and dementia. Mechanisms linking depression and cognitive decline may include increased vascular risk and activation of the innate inflammatory response. Future cohort studies are needed to test the effects of earlier life depression on cognitive outcomes in T2D. Mechanistic research is needed to define pathways by which depressive symptoms could lead to both vascular dementia and beta-amyloid accumulation. Finally, intervention studies should test whether depression is a potential target for the primary- or secondary prevention of cognitive decline in T2D.
15
Drance, Stephen M. Vascular Risk Factors and Neuroprotection in Glaucoma: Update 1996. Kugler Pubns B V (Medical), 1997.
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16
Kotseva, Kornelia, Neil Oldridge, and Massimo F. Piepoli. Evaluation of preventive cardiology. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0026.
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The Joint European Societies guidelines on cardiovascular disease (CVD) prevention define lifestyle and risk factor targets for patients with coronary or other atherosclerotic disease and people at high risk of developing CVD. However, several surveys in Europe and the United States showed inadequate lifestyle and risk factor management and under-use of prophylactic drug therapies in primary and secondary CVD prevention. Various professional associations have developed core components, standards, and outcome measures to evaluate quality of care and provide guidelines for identifying opportunities for improvements. Optimal control of cardiovascular risk factors is one of the most effective methods for reducing vascular events in patients with atherosclerotic disease or high cardiovascular risk. Improving treatment adherence is also very important. Health-related quality of life (HRQL) is considered as an outcome measure in research studies and in clinical practice. HRQL measures can help in improving patient-clinician communication, screening, monitoring, and continuous assessment of quality of care.
17
Kotseva, Kornelia, Neil Oldridge, and Massimo F. Piepoli. Evaluation of preventive cardiology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199656653.003.0026_update_001.
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The Joint European Societies guidelines on cardiovascular disease (CVD) prevention define lifestyle and risk factor targets for patients with coronary or other atherosclerotic disease and people at high risk of developing CVD. However, several surveys in Europe and the United States showed inadequate lifestyle and risk factor management and under-use of prophylactic drug therapies in primary and secondary CVD prevention. Various professional associations have developed core components, standards, and outcome measures to evaluate quality of care and provide guidelines for identifying opportunities for improvements. Optimal control of cardiovascular risk factors is one of the most effective methods for reducing vascular events in patients with atherosclerotic disease or high cardiovascular risk. Improving treatment adherence is also very important. Health-related quality of life (HRQL) is considered as an outcome measure in research studies and in clinical practice. HRQL measures can help in improving patient-clinician communication, screening, monitoring, and continuous assessment of quality of care.
18
M, Gotto Antonio, and International Symposium on Multiple Risk Factors in Cardiovascular Disease (3rd : 1994 : Florence, Italy), eds. Multiple risk factors in cardiovascular disease: Vascular and organ protection. Dordrecht: Kluwer Academic Publishers, 1995.
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19
Huang, Yuli, Zhen Yang, and Ji Bihl, eds. Cardiovascular Risk Factors: Related Vascular Injury and New Molecular Biomarkers. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-83250-313-3.
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20
Paoletti, Rodolfo, Alberico L. Catapano, Claude Lenfant, and Antonio M. Gotto Jr. Multiple Risk Factors in Cardiovascular Disease: Vascular and Organ Protection. Springer, 2012.
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21
Almedawar, Mohamad M., Richard C. Siow, and Henning Morawietz. MicroRNAs as novel biomarkers in depression, diabetes, and cardiovascular diseases. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198789284.003.0003.
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Diabetic, depressive, and cardiovascular disorders are leading causes of morbidity. In diabetics, symptoms of depression are associated with increased clinical complications. Diabetes mellitus is a major risk factor of cardiovascular diseases (CVDs). The vascular depression hypothesis suggests that CVD can increase the risk of depression or exacerbate depression-related conditions. Several studies found a strong correlation between depression and pre-existing vascular disease and vice versa. Recent studies implicate microvascular dysfunction in the pathophysiology of depression and CVD. In addition, microRNAs are potent regulators of gene expression in physiological and pathophysiological processes affecting the microcirculation. We propose an interaction between diabetes mellitus, depression, and CVD involving changes in microcirculation and microRNA expression. Hence, studies are warranted to develop novel microRNA therapeutics and biomarkers to identify diabetic patients at increased risk of developing clinical complications of depression.
22
Piggott, Margaret Ann. Neurochemical pathology of dementia. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0007.
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This chapter considers the neurodegenerative disorders Alzheimer’s disease (AD), Lewy body dementias (dementia with Lewy bodies (DLB) and Parkinson’s disease dementia(PDD)), frontotemporal dementia (FTD); and also vascular dementia (VaD) which results from cerebrovascular disease. These different conditions, which give rise to dementia syndromes, each have distinct neurochemical pathologies, with important implications for treatment. As increased age is the common risk factor generally associated with dementing illnesses, neurochemical changes are set in the context of the changes which occur during ageing. A detailed understanding of the neurotransmitter function in each condition can lead to rational drug design and treatment strategies appropriate for each group of patients. Neurochemical pathology in transmitter systems underlying clinical features of these disorders are reviewed.
23
Swanson, Karen L. Neoplastic and Vascular Diseases. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0618.
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Neoplastic and vascular disorders are reviewed. Lung cancer is the most common malignancy and cause of cancer death in both men and women worldwide. The incidence of new lung cancers has continued to decrease in men and increase in women. The risk factors include cigarette smoking, other carcinogens, cocarcinogens, radon exposure, arsenic, asbestos, coal dust, chromium, vinyl chloride, chloromethyl ether, and chronic lung injury. Genetic and nutritional factors have been implicated. Among vascular disorders, pulmonary embolism is most common. Pulmonary embolism (PE) is the cause of death in 5% to 15% of hospitalized patients who die in the United States. In a multicenter study of PE, the mortality rate at 3 months was 15% and important prognostic factors included age older than 70 years, cancer, congestive heart failure, COPD, systolic arterial hypotension, tachypnea, and right ventricular hypokinesis.
24
Hayhow, Bradleigh, and Sergio Starkstein. Biological Effects of Depression. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603342.003.0005.
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This chapter examines the bidirectional relationship between depression and stroke. It is now clearly established that depression is a significant risk factor for stroke, and vice-versa. We review the main biological and demographic factors underlying the association between stroke and depression, the predicted mortality, the mechanism of post-stroke depression, and recent findings on its pharmacological prevention. We conclude by stressing the need for developing effective strategies to manage the burden of illness associated with these interacting conditions. As with the cardiovascular system depression has major effects on the occurrence of stroke. Morbidity and mortality are increased for patients with cerebral vascular accidents (CVA) who are depressed and is seen even in a 10-year follow-up. Depression should be treated concurrently with the management of the acute phase of a CVA.
25
Karamchandani, Rahul, and Nancy R. Barbas. Vascular Cognitive Impairment. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0021.
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Vascular cognitive impairment (VCI) refers to the spectrum of cognitive disturbances that result from cerebrovascular brain injury. Cerebrovascular disease is associated with multiple underlying pathologies. Risk factors, clinical features, and treatment options overlap with those associated with Alzheimer’s disease, another common cause of cognitive decline. The complexity of vascular cognitive impairment and, notably, the interplay between clinical, pathologic, genetic, and biomarker characteristics of VCI and Alzheimer’s disease are discussed. The chapter places an emphasis on vascular cognitive impairment resulting from disease affecting small vessels, in contrast to that due to disease involving large vessels, in an effort to focus on a large body of evolving work and ongoing attempts at improving understanding of this complex entity.
26
Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.
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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.
27
Steinberg, Martin, and Paul B. Rosenberg. Cognitive Impairment and Depression in Older Patients. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199959549.001.0001.
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Depression, mild cognitive impairment (MCI) and dementia in the elderly can present with similar features such as cognitive complaints, loss of initiative, and difficulties with psychosocial functioning. These can be difficult to distinguish in the office setting, especially when mild in severity. The relationships between the three syndromes remains incompletely understood. Patients with MCI are at high risk for conversion to dementia. Depression may be either a risk factor for or early manifestation of MCI. Depression in late life is associated with Alzheimer’s disease (AD) and other dementias, but the causal relationship remains controversial. Depression may also increase the risk of conversion from MCI to dementia and be more strongly associated with conversion to Vascular dementia (VaD) than to AD. This book will provide guidance to clinicians in the diagnosis and management of these complex conditions in the office setting.
28
Steinberg, Martin, and Paul B. Rosenberg. Cognitive Impairment and Depression. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199959549.003.0001.
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Depression, mild cognitive impairment (MCI) and dementia in the elderly can present with similar features such as cognitive complaints, loss of initiative, and difficulties with psychosocial functioning. These can be difficult to distinguish in the office setting, especially when mild in severity. The relationships between the three syndromes remains incompletely understood. Patients with MCI are at high risk for conversion to dementia. Depression may be either a risk factor for or early manifestation of MCI. Depression in late life is associated with Alzheimer’s disease (AD) and other dementias, but the causal relationship remains controversial. Depression may also increase the risk of conversion from MCI to dementia and be more strongly associated with conversion to Vascular dementia (VaD) than to AD. This book will provide guidance to clinicians in the diagnosis and management of these complex conditions in the office setting.
29
Voilliot, Damien, Jaroslaw D. Kasprzak, and Eduardo Bossone. Diseases with a main influence on right ventricular function. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0060.
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As an important and independent predictive factor of morbidity and mortality, right ventricular (RV) function should be carefully assessed in patients with chronic obstructive lung disease, lung fibrosis, liver cirrhosis, or obesity. RV assessment requires a complete study of the ‘RV-pulmonary circulation unit’ with estimation of RV preload, RV intrinsic contractility, and RV afterload. Therefore, estimation of pulmonary arterial pressure, pulmonary vascular resistance, and left ventricular systolic and diastolic function should be included in this evaluation, in addition to conventional RV systolic function assessment. Three-dimensional echocardiography has emerged as an interesting tool in RV assessment and exercise echocardiography may be interesting in the risk stratification of patients.
30
Ladner, Travis R., Nishant Ganesh Kumar, Lucy He, and J. Mocco. Neuroprotection for Vascular and Endovascular Neurosurgery. Edited by David L. Reich, Stephan Mayer, and Suzan Uysal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190280253.003.0019.
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The complexity of neurovascular disease presents a challenge to the surgical and anesthesia teams managing patients with such conditions. With open or endovascular techniques, abrupt changes in hemodynamic status and intracranial pressure are an ever-present concern throughout the perioperative period. Monitoring of neurological status, hemodynamic parameters, and intracranial pressure are important adjuncts. Targeted physiologic and pharmacological interventions are critical to ensuring safe completion of complex procedures and the prevention secondary injury. This chapter reviews common complications of cerebrovascular and endovascular operations and their risk factors and summarize clinical principles, strategies, and considerations for maximizing neuroprotection in the treatment of neurovascular disease.
31
Banerjee, Amitava, and Kaleab Asrress. Screening for cardiovascular disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0351.
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Screening involves testing asymptomatic individuals who have risk factors, or individuals who are in the early stages of a disease, in order to decide whether further investigation, clinical intervention, or treatment is warranted. Therefore, screening is classically a primary prevention strategy which aims to capture disease early in its course, but it can also involve secondary prevention in individuals with established disease. In the words of Geoffrey Rose, screening is a ‘population’ strategy. Examples of screening programmes are blood pressure monitoring in primary care to screen for hypertension, and ultrasound examination to screen for abdominal aortic aneurysm. The effectiveness and feasibility of screening are influenced by several factors. First, the diagnostic accuracy of the screening test in question is crucial. For example, exercise ECG testing, although widely used, is not recommended in investigation of chest pain in current National Institute for Health and Care Excellence guidelines, due to its low sensitivity and specificity in the detection of coronary artery disease. Moreover, exercise ECG testing has even lower diagnostic accuracy in asymptomatic patients with coronary artery disease. Second, physical and financial resources influence the decision to screen. For example, the cost and the effectiveness of CT coronary angiography and other new imaging modalities to assess coronary vasculature must be weighed against the cost of existing investigations (e.g. coronary angiography) and the need for new equipment and staff training and recruitment. Finally, the safety of the investigation is an important factor, and patient preferences and physician preferences should be taken into consideration. However, while non-invasive screening examinations are preferable from the point of view of patients and clinicians, sometimes invasive screening tests may be required at a later stage in order to give a definitive diagnosis (e.g. pressure wire studies to measure fractional flow reserve in a coronary artery). The WHO’s principles of screening, first formulated in 1968, are still very relevant today. Decision analysis has led to ‘pathways’ which guide investigation and treatment within screening programmes. There is increasing recognition that there are shared risk factors and shared preventive and treatment strategies for vascular disease, regardless of arterial territory. The concept of ‘vascular medicine’ has gained credence, leading to opportunistic screening in other vascular territories if an individual presents with disease in one territory. For example, post-myocardial infarction patients have higher incidence of cerebrovascular and peripheral arterial disease, so carotid duplex scanning and measurement of the ankle–brachial pressure index may be valid screening approaches for arterial disease in other territories.
32
Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_001.
Full textAbstract:
Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
33
Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_002.
Full textAbstract:
Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
34
Elder, Grahame J. Metabolic bone disease after renal transplantation. Edited by Jeremy R. Chapman. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0288.
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Patients who undergo kidney transplantation have laboratory, bone, and soft tissue abnormalities that characterize chronic kidney disease mineral and bone disorder (CKD-MBD). After successful transplantation, abnormal values of parathyroid hormone, fibroblast growth factor 23, calcium, phosphate, vitamin D sterols, and sex hormones generally improve, but abnormalities often persist. Cardiovascular risk remains high and is influenced by prevalent vascular calcification, and fracture risk increases due to a combination of abnormal bone ‘quality’, compounded by immunosuppressive drugs and reductions in bone mineral density. Patients with well managed CKD-MBD before transplantation generally have a smoother post-transplant course, and it is useful to assess patients soon after transplantation for risk factors relevant to the general population and to patients with CKD. Targeted laboratory assessment, bone densitometry, and X-ray of the spine are useful for guiding therapy to minimize post-transplant effects of CKD-MBD. To reduce fracture risk, general measures include glucocorticoid dose minimization, attaining adequate 25(OH)D levels, and maintaining calcium and phosphate values in the normal range. Calcitriol or its analogues and antiresorptive agents such as bisphosphonates may protect bone from glucocorticoid effects and ongoing hyperparathyroidism, but the efficacy of these therapies to reduce fractures is unproven. Alternate therapies with fewer data include denosumab, strontium ranelate, teriparatide, oestrogen or testosterone hormone replacement therapy, tibolone, selective oestrogen receptor modulators, and cinacalcet. Parathyroidectomy may be necessary, but is generally avoided within the first post-transplant year. A schema is presented in this chapter that aims to minimize harm when allocating therapy.
35
Chakera, Aron, William G. Herrington, and Christopher A. O’Callaghan. Oliguria and anuria. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0056.
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Oliguria can be caused by any factor that affects renal function, or the free passage of urine down the urinary tract. Complete anuria most commonly occurs in men as a consequence of bladder outlet obstruction from an enlarged prostate. It can also arise in patients who have a single functioning kidney which then becomes obstructed or loses its vascular supply. Oliguria occurs commonly in hospitalized patients, is usually secondary to impaired renal perfusion, and is often predictable. The elderly and more unwell patients, for example, those in critical care settings, are most at risk. The presence of oliguria tends to reflect the severity of the underlying disease processes. The commonest cause of complete anuria is bladder outflow obstruction from an enlarged prostate. This may be precipitated by prostatitis or constipation in a patient with benign prostatic hypertrophy. In catheterized patients, a blocked catheter must be excluded.
36
Chong, Ji Y., and Michael P. Lerario. Young Adult with Headache and Blurred Vision. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190495541.003.0018.
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Traditional vascular risk factors such as hypertension, diabetes, and high cholesterol can contribute to stroke in young adults. In the absence of typical risk factors in a young patient, a more extensive evaluation is needed. Other, more unusual causes of stroke can include autoimmune, infectious, hematological, and toxic etiologies. Often, despite an exhaustive workup, the mechanism of stroke remains cryptogenic in younger patients.
37
Beller, Jerry, and Beller Health. 16 Dementia Types, Symptoms, and Risk Factors: Alzheimer's LBD PDD DLB FTD PPA BvFTD LATE Vascular Dementia Huntington's, Etc. Independently Published, 2019.
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38
Beller, Jerry, and Beller Health. Dementia Types, Risk Factors, and Symptoms: Alzheimer's Disease Vascular Lewy Body Frontotemporal Huntington's Normal Pressure Hydrocephalus Wernicke Korsakoff Dementias. Independently Published, 2019.
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39
Fratiglioni, Laura, and Chengxuan Qiu. Epidemiology of dementia. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0031.
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This chapter deals with the occurrence, determinants and primary prevention of dementia. Dementia is one of the major causes of functional dependence, poor quality of life, institutionalisation and mortality among elderly people. The risk of dementia increases almost exponentially with advancing age. As the population ages, dementia poses a serious threat to public health and social welfare system of our society. Accumulating evidence suggests that cardiovascular risk factors significantly contribute to the development and expression of dementia. Thus, adequate management of vascular risk factors and related disorders can be one of the preventative strategies against cognitive ageing and dementia. In addition, psychosocial factors such as educational achievement, socially-integrated and mentally-stimulating lifestyles are critical for delaying the onset of dementia by increasing cognitive reserve. Taken together, maintaining vascular health and adopting a healthy cognitive lifestyle from a life-course perspective may be the most promising strategy to achieve late-life cognitive health.
40
Selim, Magdy. Neuroprotection for General, Orthopedic, Peripheral Vascular, and ENT Surgery. Edited by David L. Reich, Stephan Mayer, and Suzan Uysal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190280253.003.0022.
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Unlike stroke after cardiac and carotid surgery, stroke after general; orthopedic; peripheral vascular; and ear, nose, and throat surgery has not been investigated extensively. The incidence, predisposing factors, and etiological mechanisms of stroke in patients undergoing these procedures are reviewed. Recommendations to prevent, recognize, and treat stroke following these surgical procedures are provided to minimize postoperative stroke risk and its associated morbidity and disability. Although these recommendations can help to decrease the incidence of perioperative stroke, there is an unmet need to find novel and effective neuroprotective strategies that can be used pre- or intraoperatively to minimize the effects of stroke on brain tissue and resulting disability. Future studies should evaluate the potential usefulness of neuroprotective therapies or interventions, including various anesthetic agents that can be used prophylactically in the perioperative setting.
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Beller, Jerry, and Beller Health. Dementia Types, Risk Factors, and Symptoms 2019: Alzheimer's Disease , Vascular , Lewy Body , Frontotemporal , Huntington's , Normal Pressure Hydrocephalus , Wernicke Korsakoff Dementias. Independently Published, 2019.
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Qiu, Chengxuan, and Laura Fratiglioni. Epidemiology of Alzheimer’s disease. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199569854.003.0003.
Full textAbstract:
• Alzheimer’s disease is the most frequent type of dementia in elderly people. An expert panel estimates that worldwide more than 24 million people are affected by dementia, most suffering from Alzheimer’s disease• The etiological factors other than old age and genetic susceptibility for Alzheimer’s disease remain to be determined, but current evidence strongly supports the potential role of vascular risk factors and psychosocial factors in the pathogenetic process and clinical manifestation of the dementing disorders...
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Raggi, Paolo, and Luis D’Marco. Imaging for detection of vascular disease in chronic kidney disease patients. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0116.
Full textAbstract:
The well-known severity of cardiovascular disease in patients suffering from chronic kidney disease (CKD) requires an accurate risk stratification of these patients in several clinical situations. Imaging has been used successfully for such purpose in the general population and it has demonstrated excellent potential among CKD patients as well. Two main forms of arterial pathology develop in patients with CKD: atherosclerosis, with accumulation of inflammatory cells, lipids, fibrous tissue and calcium in the subintimal space, and arteriosclerosis. The latter is characterized by accumulation of deposits of hydroxyapatite and amorphous calcium crystals in the muscular media of the vessel wall, and is believed to be more closely associated with alterations of mineral metabolism than with traditional atherosclerosis risk factors. The result is the development of what appears to be premature arterial ageing, with loss of elastic properties, increased stiffness, and increased overall fragility of the arterial system. Despite intensifying research and increasing awareness of these issues, the underlying pathophysiology of the aggressive vasculopathy of CKD remains largely unknown. As a consequence, there are currently very limited pathways to prevent progression of vascular damage in CKD. The indications, strengths and weaknesses of several imaging modalities employed to evaluate vascular disease in CKD are described, focusing on coronary arterial circulation and the peripheral arteries, with the exclusion of the intracranial arteries.
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Cassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Miranda Payne, Gareth Morris-Stiff, and Madhumita Bhattacharyya. Gynaecological cancers. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199689842.003.0020_update_001.
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Genitourinary cancers examines the malignancies arising in the kidney, ureter, bladder, prostate, testis, and penis. Renal cancer has high propensity for systemic spread, largely mediated by overexpression of vascular endothelial growth factor (VEGF). Treatments include surgery, immunotherapy, and targeted therapy. Wilms tumour, a childhood malignancy of the kidney, warrants specialist paediatric oncology management to provide expertise in its unique pathology, staging, and treatment, often with surgery and chemotherapy. Cancer of the bladder and ureters, another tobacco related cancer, may present as either superficial or invasive disease. The former is managed by transurethral resection and intravesical therapy. The latter may require radical surgery, preoperative chemotherapy, or radiotherapy. Prostate cancer, the commonest male cancer, is an androgen dependent malignancy. It has attracted controversy with regards to PSA screening, and potential over treatment with radical prostatectomy. Division into low, intermediate, and high risk disease according to tumour grade, stage, and PSA helps in deciding best treatment, antiandrogen therapy for metastatic disease, radiotherapy and adjuvant hormone therapy for locally advanced disease, either surgery or radiotherapy for early intermediate risk disease, and active monitoring for low risk cases. Testicular cancer divides according to pathology into seminoma, nonseminomatous germ cell tumours (NSGCT), and mixed tumours, the latter two frequently producing tumour markers, alpha-fetoprotein (AFP) and/or human chorionic gonadotrophin (HCG). Stage I disease is managed by inguinal orchidectomy and surveillance or adjuvant chemotherapy. More advanced disease is managed by chemotherapy, with high probability of cure in the majority. Penile cancer, often HPV related, can be excised when it presents early, but delay in presentation may lead to regional and systemic spread with poor prognosis.
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Qiu, Chengxuan, and Laura Fratiglioni. Epidemiology of Alzheimer’s disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198779803.003.0003.
Full textAbstract:
This chapter provides a brief overview concerning the global epidemic, risk and protective factors, and possible intervention strategies of Alzheimer’s disease, the most common type of dementia. Alzheimer’s disease, which is projected to reach global epidemic level in three to four decades, already has a huge economic and societal impact. Epidemiologic research has provided sufficient evidence supporting that lifestyle or cardiovascular risk factors in middle-aged and older adults play a critical role in the onset and progression of late-life dementia and Alzheimer’s disease, whereas active engagement in mental, social, and physical activities may postpone the onset of the dementing disorders. The community intervention studies are warranted to determine to what extent intervention strategies towards control of major lifestyle and cardiovascular risk factors and related vascular disorders as well as maintenance of an active lifestyle may help delay the onset of Alzheimer’s disease and dementia syndrome.
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Chong, Ji Y., and Michael P. Lerario. Seeing Jellyfish. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190495541.003.0021.
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Migraine may mimic stroke, but acute migraine can also be a (rare) cause of stroke, particularly in the posterior circulation. This risk is particularly high in patients who experience migraine aura, or in those who are smokers or who take oral contraceptives. Because this is a diagnosis of exclusion, other etiologies of stroke need to be investigated. Although there are no high-level clinical trial data, it is advised to control vascular risk factors and avoid medications that can potentially induce vasoconstriction in patients with migraine-related stroke.
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Speer, Thimoteus, and Danilo Fliser. Abnormal endothelial vasomotor and secretory function. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0113.
Full textAbstract:
The endothelium plays a crucial role in the maintenance of vascular integrity and function. Nitric oxide produced by endothelial cells is a key player, inducing relaxation of vascular smooth muscle cells, inhibition of vascular inflammation, and prevention of coagulatory activation. Chronic kidney disease (CKD) is characterized by deterioration of different protective endothelial properties, collectively described as endothelial dysfunction. Several factors such as methylarginines, modified lipoproteins, and other substances that accumulate may be involved in the pathogenesis of endothelial dysfunction of CKD. Endothelial dysfunction is suggested to be the first critical step in the initiation of atherosclerosis. Clinical assessment of endothelial function may become important in recognition of patients with increased cardiovascular risk. Beside several invasive and non-invasive methods to assess endothelial function in vivo, measurement of circulating (bio)markers may be useful for the evaluation of endothelial dysfunction.
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Barnard, Matthew, and Nicola Jones. Intensive care management after cardiothoracic surgery. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0368.
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Management of the post-cardiothoracic surgical patient follows general principles of intensive care, but incorporates certain unique considerations. In cardiac surgical patients peri-operative ischaemia, arrhythmias and ventricular dysfunction mandate specific monitoring requirements, and individual pharmacological and mechanical support. Suspicion of myocardial ischaemia should not only lead to pharmacological treatment, but also consideration of urgent angiography to exclude coronary graft occlusion. Ventricular dysfunction may be pre-existing or attributable to intra-operative myocardial ‘stunning’. Catecholamines and phosphodiesterase inhibitors are the mainstay of therapy. Rarely, intra-aortic balloon pumping or ventricular assist devices are required. Significant bleeding (with potential cardiac tamponade), respiratory compromise, acute kidney injury, neurological injury, and deep sternal wound infection each occur in ~2–3% of cardiac surgical patients. Each of these has individual risk factors and specific management considerations. General guidelines for patients who have undergone thoracic surgery include early extubation, fluid restriction, effective analgesia, and protective lung ventilation. Thoracic patients are at risk of atelectasis, respiratory infection, bronchial air leak, and right ventricular failure. Positive pressure ventilation is avoided whenever possible particularly after pneumonectomy, but is sometimes necessary in compromised patients. Air leaks are common. Alveolopleural fistulae usually improve with conservative management,whereas bronchopleural fistulae are more likely to require surgical intervention. Lung surgery is high risk for patients with ischaemic heart disease. Patients with pre-existing elevated pulmonary vascular resistance may exhibit right ventricular dysfunction and may fail to cope with a further increase in pulmonary vascular resistance consequent to lung resection. Lung collapse and infection are constant risks throughout the entire post-operative period.
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Delcourt, Candice, and Craig Anderson. Epidemiology of stroke. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0234.
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Approximately 20 million strokes occur in the world each year and over one-quarter of these are fatal. This makes stroke the second most common cause of death, after ischaemic heart disease, and strokes are responsible for 6 million deaths (almost 10% of all deaths) annually. Stroke has major consequences in terms of residual physical disability, depression, dementia, epilepsy, and carer burden. Moreover, around 20% of survivors experience a further stroke or serious vascular event within a few years of the index event. The economic and societal costs of stroke are enormous. With ongoing demographic changes, including the ageing and urbanization of populations, and persistence of highly prevalent risk factors related to adverse lifestyles, the global burden of disease related to stroke is predicted to rise substantially by 2030.
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Morris, Rhiain. Psychological management of coronary heart disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0123.
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Both anxiety and depression have been found to increase the risk of developing coronary heart disease (CHD) and lead to exacerbation of cardiac symptoms, with the latter subsequently impacting recovery/rehabilitation (e.g. leading to an increased number of readmissions to hospital, and an increased mortality risk following myocardial infarction (MI)). This may be due to pathophysiologic effects, such as vascular inflammation and autonomic dysfunction, and poor lifestyle/behavioural patterns, including non-attendance at cardiac rehabilitation classes; and/or poor treatment adherence. Psychosocial factors such as stress, hostility, social isolation, socio-economic status, and psychological defensiveness can also affect the course of cardiac illness.